Acetazolamide and CO2 in hyperbaric oxygen toxicity.
The role of CO2 in hyperbaric oxygen toxicity was investigated by administering acetazolamide (Diamox), Tris buffer [tris(hydroxymethyl)aminomethane], and sodium bicarbonate by i.p. injection, and by exposure of other groups of animals to an atmosphere of 5% CO2 and 95% O2. All animals were placed in a pressure chamber and maintained at 50 psig in 100% O2 until death. The Tris buffer and the sodium bicarbonate buffer significantly extended time to onset of convulsions and to time of death. Acetazolamide and also 5% CO2 shortened time to onset of convulsions and significantly shortened survival time. These results suggest that increased tissue levels of CO2 play an important role in hyperbaric oxygen toxicity. The cause of death in our animals exposed to hyperbaric oxygen was pulmonary edema secondary to a systemic hypertension.
D000086:Acetazolamide / Q000494:pharmacology*; D000818:Animals; D001469:Barotrauma / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000494:pharmacology*; D006931:Hyperbaric Oxygenation; D008297:Male; D010100:Oxygen / Q000633:toxicity*; D051381:Rats; D011919:Rats, Inbred Strains; D012640:Seizures / Q000209:etiology; D013997:Time Factors
D002245:Carbon Dioxide; D000086:Acetazolamide; D010100:Oxygen